Effects of ionising radiation exposure in offspring and next generations: dosimetric aspects and uncertainties

Abstract

Purpose

The impact of the exposure to ionizing radiation in the offspring and next generation has been investigated in the last decades and currently is the subject of study of the ICRP Task Group 121. Studying the effects of radiation exposure in pre-conceptional and post-conceptional phases can be a challenge since potential effects to the fetus vary depending on the stage of fetal development. Epidemiology and radiobiology studies are the two sources of information one can use to correlate the radiation dose to the human body and tissues and the resulting effects. For a proper evaluation of the outcomes of such studies, and a correct appraisal of the exposure/dose-effect relationship, (i) reliable dosimetry, (ii) accurate reporting, and (iii) reproducibility of results are required. Although variables related to dose, including for instance source of radiation, geometry of irradiation, dose rate etc., are usually known, especially in radiobiology studies, often important details of the irradiation are not reported.

Conclusions

Based on standards developed by the National Cancer Institute (NCI), the National Institute of Allergy and Infectious Disease (NIAID) and the National Institute of Standards and Technology (NIST), a review of the scientific studies used by the UNSCEAR to estimate the risk of hereditary effects, and by the ICRP in its current recommendations, was conducted to evaluate the way dosimetry was reported. Dosimetry and the related uncertainties were not adequately described in the vast majority of those studies. This does not necessarily mean that they do not provide relevant information, however it prevents from a thorough verification and reproduction of their findings. In order to guarantee the reliability and robustness of the process of revision of the estimates of risk and detriment it is therefore considered mandatory to include a careful check of the new relevant literature with regard to the criteria on the completeness and reproducibility of the dosimetric information.

Keywords:

• Fetal dosimetry
• uncertainties
• pre-conceptional exposure
• post-conceptional exposure
• offspring

Introduction

The effects of ionizing radiation exposure in offspring and next generations may arise great interest not only among radiation researchers and professionals, but also among the general population. During childbearing years, many individuals become more aware of hazards in their environment that could affect their ability to have healthy children. Moreover, pregnancy can be a delicate moment which imposes a level of personal responsibility that is intense and unique (Marx 2018). Addressing uncertainties on the risks related with pre-conceptional and post-conceptional exposures to ionizing radiation, including the dosimetric aspects, are essential when defining dose thresholds and dose-response curves.

Although it is known, primarily from mammalian animal studies, that the developing fetus is sensitive to ionizing radiation, it is currently considered that doses less than 0.1 Gy do not increase the risk of lethality or malformations in the developing fetus (NCRP 2013; CDC 2019; ICRP 2003, 2007).

However, studying the effects of radiation exposure in pre-conceptional and post-conceptional phases can be a challenge. When studying the effects of radiation exposures in the pre-conceptional phase it is essential to account for the time before the pregnancy that the parents were exposed, specifically in relation to the dose to the gonads. It also is important to consider whether just the mother/father was affected or both. This is particularly challenging in the case of internal exposures, as the gametes can be irradiated also for long times after the incorporation. For post-conceptional exposures, potential effects to the fetus vary depending on the stage of fetal development and on the magnitude of the radiation doses received.

Reliable dosimetry techniques and accurate reporting on them and on the associated uncertainties are necessary to ensure reproducibility of the results, proper evaluation of the outcomes of such studies and thus a correct appraisal of the exposure/dose-effect relationship. Meta-analyses of radiobiology studies (Desrosiers et al. 2013; Draeger et al. 2020) have actually pointed out poor description of the dosimetry information as a common drawback of such studies. For example, oftentimes it is unclear which dose is being reported—whether dose to the total body or dose to a specific tissue or to an organ. Additionally, some epidemiology studies may rely on the analysis of old cases with poorly known information on the exposed scenarios.

These uncertainties add up to the more general issues affecting these analyses, for instance to which extent the results of controlled studies with cellular or animal models can be extended to human populations.

Risk estimation of hereditary effects

As discussed by Amrenova et al. in another contribution to this issue (‘Consideration of hereditary effects in the radiological protection system: evolution and current status’), the method proposed by the ICRP 103 (ICRP 2007, UNSCEAR. 2001) to evaluate the risk of hereditary effects is expressed by the following equation: (1) $$\text{Risk per unit dose =}{\sum }_{\mathrm{D}}{\mathrm{P}}_{\mathrm{D}}\mathrm{\times }\left[\frac{1}{{\text{DD}}_{\mathrm{D}}}\right]\mathrm{\times }{\text{MC}}_{\mathrm{D}}\mathrm{\times }{\text{PRCF}}_{\mathrm{D}}$$(1) being: ‘D’ the class of genetic diseases; ‘P’ the baseline frequency of the disease class; ‘DD’ the doubling dose (required amount of radiation to produce an increase in frequency equivalent to P); ‘MC’ the disease-class-specific mutation component (relative increase in disease frequency per unit relative increase in mutation rate); and, ‘PRCF’ the potential recoverability correction factor. This approach does not apply to the risk of congenital abnormalities, which is estimated without recourse to the doubling dose concept.

The quantity of dosimetric interest in equation (1)(1) $$\text{Risk per unit dose =}{\sum }_{\mathrm{D}}{\mathrm{P}}_{\mathrm{D}}\mathrm{\times }\left[\frac{1}{{\text{DD}}_{\mathrm{D}}}\right]\mathrm{\times }{\text{MC}}_{\mathrm{D}}\mathrm{\times }{\text{PRCF}}_{\mathrm{D}}$$(1) is DD_D, i.e. the required absorbed dose to the reproduction organs to produce as many hereditary mutations as those arising spontaneously in a generation. The estimate of the doubling dose is currently based on the comparison of human data on spontaneous mutation rates with data on induced mutation rates from experiments involving irradiation of male mice (Sankaranarayanan and Chakraborty 2000; UNSCEAR 2001). The data from female mice have not been used, as mouse immature oocytes were not considered to be a good model for human immature oocytes (Neel and Lewis 1990).

The assessed value of (0.82 ± 0.29) Gy for low-LET, low dose chronic irradiation was considered to be consistent with the previously assumed value of 1 Gy (UNSCEAR 1993), estimated exclusively from mouse data for both spontaneous and induced mutation rates. Under consideration of the associated uncertainties, DD_D was confirmed equal to 1 Gy for all hereditary diseases.

In the following we are not going to discuss the opportunity of these assumptions regarding the DD_D, as this aspect is already addressed elsewhere in this journal issue, and will focus our attention on the dosimetric aspects of the studies used to obtain the estimates of induced mutations in different species.

Post-conceptional effects

Potential radiation effects vary depending on the stage of fetal development and on the magnitude of the radiation doses received. The fetus is most sensitive to radiation during the first weeks after conception. As a pregnancy progresses, the dose associated with adverse reproductive effects increases (that is, it takes a higher dose to cause an adverse reproductive effect), until about 20 weeks into the pregnancy. Beyond the 20th week of pregnancy, the fetus has become more resistant to the developmental effects of radiation. In fact, the fetus is probably no more vulnerable to many of the effects of radiation than the mother in the later part of pregnancy (HPS 2022).

For many years researchers could not trace dose-effect relationships in many of the animal studies. This is the reason why they thought that malformations induced by radiation exposure during the pre-implantation period were not likely to happen and that lethality of the embryo would be the only outcome from such exposures (ICRP 2003). During the 1950s, Russell (1956) proposed the ‘all-or-none rule’, claiming that radiation exposures of embryos before the organogenesis would result in either no harmful effect or in embryonic death. Based on data available at that time, the ICRP concluded in its Publication 90 (ICRP 2003) that the embryo is susceptible to lethal effects of radiation during the pre-implantation period and that at doses under 100 mGy lethal effects are not very often reported.

Concerning the in-utero radiosensitivity, they also concluded that it was possible to trace a gestational age-dependency relationship, being the period of major organogenesis the most sensitive period. Based on animal data, for the induction of malformations a dose threshold around 100 mGy was observed. Thus, they considered that risks of malformations after in-utero exposure to doses below 100 mGy are not expected.

A threshold dose of 300 mGy in the most sensitive prenatal period (8-15 weeks post conception) is supported by the observations in A-bomb survivors. ICRP assumed that in the absence of a true threshold for effects on Intelligence Quotient (IQ) following in-utero exposures, doses under 100 mGy would be of no great significance (ICRP 2003).

The studies considered by ICRP in the Publication 90 (ICRP 2003) were mainly published during the period from 1950 to 1980. These studies (Job et al. 1935, Russel 1957, Rugh and Grupp 1959, Hicks and D’Amato 1963, Ohzu 1965, Jacobsen 1968) were strongly criticized by Mole in the beginning of the 1990s due to the lack of: (i) a proper description of how dose thresholds were determined, (ii) the fact that assumptions were made based on experimental studies with limited dose-dependence outcomes, (iii) and presence of other confounding factors involved in the experiments that could impact the results of the research (Mole 1992). Even though over 30 years have passed, some of the issues remain present and some questions remain unanswered.

Importance and peculiarities of dosimetry

Epidemiology and radiobiology studies are by large the two main sources of information to trace the correlation between the radiation dose to the human body, tissues or cells and the resultant effects. This correlation is usually called dose-response and can be graphically represented by a curve that relates the amount of dose delivered to the human/animal body, tissue or cell and its respective effect. Knowledge of this correlation also helps defining a dose threshold to a specific effect, if any. The dose is therefore the crucial input information of this analysis, and it should be evaluated and reported as accurately and precisely as possible. Failing that, any consideration on the resulting effects is likely to be inconclusive.

Many factors play a role in the dose assessment process and need to be not only assessed in the studies, but also correctly reported in order to be able to be verified and/or replicated. An extensive, but not exhaustive, listing includes among others (Desrosiers et al. 2013; Draeger et al. 2020; NCRP 2019a):

• Source specification:

  • type and energy;

  • for x-ray sources: beam quality, voltage setting, filter materials and thicknesses, measured half-value layer (HVL), radiation spectrum;

  • for radioactive sources: shape and casing, calibrated activity, assumed half-life;

  • in case of intake of radionuclides material solubility and other physico-chemical characteristics.

• Irradiation aspects:

  • calibration procedure including published standards/protocols used;

  • geometry set-up: beam size and orientation, distance from the source;

  • backscatter;

  • dose rates and dose fractionations;

  • duration of the exposure;

  • partial or whole-body exposure;

  • homogeneity of the exposure;

  • environmental parameters (temperature, relative humidity).

• Dosimetric aspects:

  • the type of dose considered: absorbed or equivalent dose to a specific organ or tissue, effective dose; dose in air, water, plastic, tissue;

  • dosimetry equipment and techniques used.

• Mathematical aspects:

  • models and software used to estimate dose in case of lacking relevant measurements.

The timing of the exposure is another important issue for a correct definition of the dose-effect relationship. In this instance, for hereditary effects it must be noted that whereas a female is born with all reproductive cells (oocytes) which she will carry in her ovaries during her lifetime, male germ cells are continuously produced. Therefore, exposures dating back a long time and cumulated doses to gonads due to chronic radiation exposures are mainly relevant for primordial oocytes only. In case of post-conceptional phase, it is important to identify in which embryonic/fetal age the exposure happened.

In case of incorporation of radionuclides by the mother there are additional peculiarities to be considered. The embryo and fetus are irradiated by the activity present in the mother’s body. Activity transferred to the developing organism via placental transfer may remain in the newborn organism also after delivery. The additional exposure after birth needs thus to be taken into account in the interpretation of the results. This scenario differs from the one of an external exposure since: (i) the irradiation continues as long as the radionuclides are in the body of the mother, the embryo/fetus and/or the newborn, (ii) it is spatially and temporally inhomogeneous, with generally low, but time-varying dose rates, (iii) a significant portion of the dose may be due to the absorption of beta and alpha particles emitted in the body, with different properties and efficacy than photons, usually the predominant source for external irradiations.

Uncertainties in internal dose assessments can be associated to the poor characterization of the radionuclide in terms of the particle size distribution of a radioactive aerosol and of the solubility of the aerosol in the respiratory or alimentary tract, and/or when taken up through a wound. The route of intake is also an important detail to the dose assessment, and sometimes it is not known if the intake occurred by ingestion or/and inhalation. Other uncertainties derive from the assumptions made on the model, whether the model was based on human data or animal data, and whether the model was based on the specific element of concern or based on an element assumed to have similar biokinetics. Lastly, the individuals in a population are not an exact replica of the reference models considering the anatomy and the physiology.

In the case of epidemiologic studies, doses are usually assessed retrospectively. The source of random errors or systematic errors in radiation epidemiologic studies that could lead to unreliable dose-response curves and dose thresholds are:

• classical measurement of error – when estimating individual dose from measurements or a dose reconstruction that makes use of questionnaires to estimate doses,

• Berkson measurement error – represent variability of individuals’ true doses about an unbiased assigned dose or dose factor, and

• shared error – address the issue that the assigned average dose of dose-factor coefficients themselves have uncertainties.

The dose estimates should be as much as individualized as possible to reduce the uncertainties of the study, to shape the dose-response curve and to enforce the statistical power due to the range of individual exposures. Nonetheless, uncertainties in personal reporting, lack of statistical adjustments for confounders, dose-related inequalities in disease findings (e.g. different values of dose thresholds), errors in assigning average values for dosimetry parameters are among the factors that should be considered (NCRP 2012). According to Gilbert (2009), errors that are independent from subject to subject reduce statistical power for detecting a dose-response relationship, increase uncertainties in estimated risk coefficients, and may lead to underestimation of risk coefficients.

To ensure reliability of the dose-response curves and dose thresholds, it is also necessary to trace and minimize all sources of uncertainties associated to the aspects listed above, identifying the role they play in the final dose assessment. NCRP Reports 163 and 164 (NCRP 2009a, 2009b) details steps and foundation elements of the dose-reconstruction process in the case of epidemiology studies, as well as the source of uncertainties for each dose estimate component.

Radiobiology studies are in principle not affected by such difficulties as they are conducted in controlled environments: the source of radiation, the type of the radiation, the dose rate, the type of exposure (single or chronic), the mass of the exposed tissue, the length of exposure among other parameters are known. Nevertheless, these studies are conducted on cells or animals of other species (mice, rats, guinea-pigs) and the translation of the results to the human species can be challenging, adding a further source of uncertainty. On top of that, recent analyses have shown that also in radiation biology studies, when all exposure conditions were controlled and therefore known, very often dosimetry was not accurately or only partially reported at the time of publication (Desrosiers et al. 2013; Draeger et al. 2020). Among the findings which are worth mentioning, the source of radiation and the equipment used to measure the dose were reported in less than 16% of the cases, and only 1.2% mentioned the calibration protocol. The fractionation schedule was mentioned by less than 30% of the authors, and other important irradiation parameters like the field size, the distance to the source and the attenuation or backscatter material were described by less than 20% of the authors (Draeger et al. 2020). This makes it difficult to evaluate the appropriateness of the dose estimates and severely affects the reproducibility and translatability of the results. This deficiency in reporting essential experimental data is among the possible causes of what has been called the reproducibility crisis of these studies, i.e. the fact that frequently studies conducted under similar experimental conditions by different groups lead to different results. But precisely, if details of the experimental setting are missing or imprecise, it is impossible to completely replicate the conditions under which the study was conducted and it is therefore inevitable to arrive at conflicting results.

Doubling dose for hereditary effects

The estimate of DD_D presented by Sankaranarayanan and Chakraborty (2000) is based on a number of studies involving irradiation of male mice (Cattanach et al. 1985; Cattanach and Moseley 1974; Cattanach and Rasberry 1994; Charles and Pretsch 1986; Lyon and Morris 1969; Lyon et al. 1964, 1972a, 1972b; Phillips 1961; Pretsch et al. 1994; Russell 1956, 1957, 1965, 1968; Russell et al. 1958). In this analysis mutation rates were normalized to single acute X-irradiation conditions for the sake of comparison. The radiation-induced mutation rate for chronic low LET radiation was assessed using a dose-rate reduction factor of three.

As indicated before, we are not going to discuss the derivation of the doubling dose value, rather we have checked how the dosimetry was reported in the mentioned studies. For that we have considered the standards proposed by Desrosiers et al. (2013).

The first relevant studies in the field are those of the Russell and Russell group. The description of the exposures in those studies was as follows:

Young mature male mice were exposed, in polystyrene cages of 3.0 to 3.5-millimeter wall thickness […] to a 5-Ci ¹³⁷Cs source. Dose rate was regulated by distance. Exposure was continuous […] until the total dose had been accumulated. (Russell et al. 1958).

Comparing to the list of criteria mentioned before, we note that there is lack of information useful to reproduce the study (e.g. time of exposure, field size, number of exposures, distance to the source, filtration).

The great majority of the mentioned studies involved exposures to 250 kVp-X-rays as well as ⁶⁰Co and ¹³⁷Cs sources. Sufficient details about source specification and irradiation parameters (in case of X-irradiation: energy, applied voltage, dose rates used, fractionation scheme, half-value layer, sometimes applied filtration), but not on field size, beam direction, distance from source, backscatter or calibration protocols are given. The doses reported by Lyon et al. (1964), Lyon and Morris (1969), Cattanach and Moseley (1974), Cattanach et al. (1985) and Cattanach and Rasberry (1994) are referred to exposures of the ‘posterior third of the body’, without further specifications, and in some earlier papers the values are expressed in roentgen (R). Charles and Pretsch (1986) indicate more specifically that the anterior part of the body was protected by a lead shield, without any consideration given to the possible effects of scattered radiation. In other papers (Lyon et al. 1972a, 1972b) whole-body exposures in rad are mentioned, without further specifications.

From the information provided it not possible to infer the accuracy of the reported doses without any details on how they were assessed (calibration protocols, instrumentation used, quality assurance measures). The type of dose is not explicitly specified: is it a whole-body dose, also in case of partial-body irradiation? Or are there doses to relevant organs, like the gonads? It is also difficult to assess to which extent the exposure of the animals was uniform without further specification of beam size and orientation, distance between source and target (animals) and other information on animal caging (e.g. to which extent they were allowed to move during the irradiations, which were of different durations, so modifying the irradiation geometry).

Finally, the necessity of having to revise, decades later, the analyses due to some unclear issues with the reporting of the results and with how to consider spontaneous mutations which originated as germinal mosaics, what led some authors to review and re-publish their studies some decades later (Russell and Russell 1992; Selby 1998, 2020) poses a further challenge to the reliability of these studies.

Further to that, the assumption to use a dose-rate reduction factor of three used by Sankaranarayanan and Chakraborty, however plausible, is only justified by general considerations and would need further investigation.

Studies on post-conceptional exposures

The assumptions and motivation behind the estimates of risks due to post-conceptional exposures were already questioned at the beginning of the 1990s (Mole 1992). In that work the author criticized what was known about the sensitivity of the embryo and fetus to ionizing radiation and the most important assumptions made at that time regarding the teratogenic effects of radiation based on animal data. Especially the lack of a clear dose-response relationship and of a sound control data were indicated as major flaws of that analysis.

Moreover, different strains in the same species are expected to develop different degrees of functional disability in organs when exposed to radiation. These differences occur due to differences on the susceptibility that each strain has to to develop different functional disabilities, thus, they should not be directly compared. In the same manner, comparing such degrees of disability directly between different species (e.g. rodent and human) is not reliable.

Most of the criticism of the Mole paper was directed to the choice of the endpoints considered for the risk/detriment assessment. Mole noted that most of the experimental information about effects of post-conceptional exposure to ionizing radiation not only refers to laboratory animals, but was also collected at a time when knowledge of functional development in mammals was not yet understood. According to the review, teratogenic effects at that time were usually recorded regarding what was externally visible, but major malformations could have been lethal right after birth, and minor malformations would not be lethal at all. Death of the fetus during its development could cause malformations to remain undetected unless with detailed internal examinations, again potentially biasing the result of the analysis.

Beyond the methodological issues highlighted by Mole (1992), we also revisited the references mentioned in his paper to look over the dosimetric information according to the criteria listed by Desrosiers et al. (2013) on the requirements to ensure reproducibility of radiobiology studies. Table 1 shows the result of the evaluation. In some of those studies exposures in R (Roentgen), and not doses, were reported, so the papers were checked for the information they provided on exposure. Mole himself did not differentiate dose and exposure in his article, and considered the reports from the authors as dose, however using R as unit. To allow a better understanding of the Table, exposure values were converted to dose to soft tissues. The conversion factor between these two quantities is 1 R = 0.0096 Gy. For simplicity, and to avoid giving the false impression of extreme precision in the exposure values, it was rounded up to 0.01. For those studies in which the dose has been reported in rad (r), the value was similarly converted to Gy with a conversion factor of 1 r = 0.01 Gy.

Table 1. Synopsis of the lowest teratogenic doses observed in mice and rats (Mole 1992) and the parameters that were missing according to the Desrosiers et al. (2013) standards for dosimetric report.

Reference	Day of exposure (p.o.)^§	Exposure reported by the authors (R)	Dose reported by the authors (r)	Dose (Gy)*	Effects observed	Missing parameters
Rugh and Grupp 1959	0.5	–	5	0.05	Increase in resorption frequency	Size of the field, calibration, backscatter, equipment used to measure the dose
	0.5–1.5	–	15–20	0.15–0.20	Exencephaly
Ohzu 1965	0.5–1.5	5	–	0.05	Polydactilia	Calibration, backscatter, equipment used to measure the exposure. The author refers to dose but the results are shown in R
	7.5	5	–	0.05	Increase in resorption frequency
Jacobsen 1968	7.5	5	–	0.05	Skeletal malformations	All the parameters are missing. The author refers to dose but all the results are shown in R
	7.5	5	–	0.05	Decrease in litter weight
	7.5	5	–	0.05	Hydramnios
	7.5	5	–	0.05	Reduced tail length
Russel 1957	7.5–8.5		25	0.25	Malformation of the axial skeleton	Size of the field, calibration, backscatter equipment used to measure the dose, dose rate
Murakami and Kameyama 1958	8.5		25	0.25	Hydrocephalus, flexion of the spinal cord, architectural changes in ependymal cells	Size of the field, calibration, backscatter, equipment used to measure the dose
Majima 1961	8.5		50	0.50	Eye defects	Size of the field, calibration, backscatter, equipment used to measure the dose
Brent 1960	0–8		5–25	0.05 − 0.25	Growth disturbances	All the parameters are missing
Wilson 1954	8		12.5	0.125	Growth disturbances	Dose rate, equipment used to measure the dose
Job et al. 1935	8–9		36–40	0.36–0.40	Ocular and cerebral malformations	Size of the field, calibration, backscatter, equipment used to measure the dose
Wilson and Karr 1951	9		50	0.50	Growth disturbances	Dose rate, equipment used to measure the, dose
Wilson et al. 1953	9		50	0.50	Increase in resorption	Dose rate, equipment used to measure the dose
Wilson 1954	9		12.5	0.125	Ocular and cerebral malformations	Dose rate, equipment used to measure the exposure.
	9		100	1	Heart and aortic, face, and urinary tract malformations
	9		50	0.50	Brain and spinal cord malformations
	9		25	0.25	Microphtalmia, anophtalmia
Hicks and D’Amato 1963	16–22		10–40	0.10–0.40	Permanent alterations of nerve cells and cortical architecture of the brain	All the parameters are missing

*Calculated by the authors (rounded values).

^§p.o. = post ovulation.

Although information on the exposure/dose rate, equipment to measure the exposure/dose, and subject size were still missing, the series of studies published by Wilson and Karr (1951), Wilson et al. (1953) and Wilson (1954) is the one that comes closest to the standards established by Desrosiers et al. (2013) in terms of describing dosimetric factors to ensure the reproducibility of the study. It is important to stress again that the lack of such information does not necessarily invalidate the outcomes of the studies, however it complicates their verification and makes it impossible to replicate them.

Summary and conclusions

In this contribution, we have discussed the crucial role played by dosimetry in the assessment of the dose-effect relationship and how important it is to provide all necessary background information in order for the reader to be able to correctly interpret the dosimetry results reported and evaluate the reliability and reproducibility of the dose assessment. It is imperative that the readers are presented with complete information so they can clearly understand how the dosimetry was performed and the meaning of the results. This study has clearly pointed out that the dosimetry and the related uncertainties were not adequately reported in the vast majority of the studies which have been used to assess risk and detriment for pre- and post-conceptional exposures in the current ICRP recommendations. This does not necessarily mean that these studies do not provide relevant epidemiological or radiobiological information, and that the estimates and assumptions made in the recommendations are per se incorrect, however it prevents from a thorough verification and reproduction of those findings.

A consistent number of epidemiology and radiobiology studies have been published since the analysis which is at the basis of the current ICRP recommendations, providing new or updated valuable information to inform the currently ongoing revision process. In order to have a solid basis for the estimates of risk and detriment, the revision process needs to include a careful check of these new studies also with regard to the criteria on the completeness and reproducibility of the dosimetric information, as presented here.

Disclosure statement

The authors declare that there are no relevant financial or non-financial competing interests to report.

Additional information

Notes on contributors

Ämilie Degenhardt

Ämilie Degenhardt, PhD, is a postdoctoral fellow in the Unit ‘External and internal dosimetry, biokinetics’ at the Department of Medical and Occupational Radiation Protection of the German Federal Office for Radiation Protection (BfS), Oberschleißheim, Germany.

Sara Dumit

Sara Dumit, PhD, is a Scientist at the Internal Dosimetry Group of the Radiation Protection Division at Los Alamos National Laboratory (LANL), Los Alamos, United States of America.

Augusto Giussani

Augusto Giussani, PhD, is the Head of the Unit ‘External and internal dosimetry, biokinetics’ at the Department of Medical and Occupational Radiation Protection of the German Federal Office for Radiation Protection (BfS), Oberschleißheim, Germany.